Abstract
Objective To observe the protective effect of etomidate postcoditioning on transient focal cerebral ischemiareperfusion (I/R) injury in rats. Methods Thirty-two male Sprague-Dawley rats (six months, body weight between 250 g~300 g)were randomly divided into four groups (n=8): Sham group,I/R group, L group (lipid), Eto group (etomidate). Ischemia were induced by occluding the right middle cerebral artery in rat for 2 h. In I/R group, L group and Eto group, saline, lipid (the vehicle solution of etomidate )or etomidate(20 mg/kg)( the volume was fixed to 1 ml/100 g )were administered intraperitoneally immediately to rats at the onset of reperfusion respecetively. The neurological outcomes were evaluated after reperfusion 12,24 and 72 h by modified neurologic severity scores (NSS). The infarct size of brain was then assessed by 10 g/L 2,3,5-triphenyltetrazolium (TTC) staining following the last neurological outcome evaluation. Results The neurologic severity scores in Sham group was 0 at the three time points, and the neurologic severity scores in I/R group and L group at reperfusion 12,24 and 72 h were significantly more than those in Sham group (0)and Eto group (P<0.05), there was no significant difference between I/R group and L group (P>0.05 on 12, 24,72 h ). The infarct size of brain in I/R group(40.1±2.3 )% and L group (39.3±2.1)% were evidently greater than that in Sham group (0) and in Eto group (26.0±4.9)% (P<0.05) at reperfusion 72 h, and there was no significant difference between I/R group and L group( P>0.05 ). Conclusion Etomidate( 20 mg/kg ) has a brain protective effect on cerebral inschemia-reperfusion injury in rats. Key words: Etomidate; Postcoditioning; Cerebral ischemia-reperfusion; 2,3,5-triphenyltetrazolium
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